Epidemic Strain Shigella dysenteriae Type 1 Dt66 Encodes Several Drug Resistances by Chromosome

Hens, Dipak Kumar; Niyogi, Swapan Kumar; Kumar, R.

doi:10.1016/j.arcmed.2005.03.006

Cited by 5 publications

(2 citation statements)

References 28 publications

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“…Since the 1960s, S. dysenteriae type 1 is known to be an important cause of epidemic dysentery in Latin America, Africa, and Asia, including Bangladesh (1,3-6). Epidemic shigellosis largely depends on drug resistance (7), variation in Shiga toxin (8), or other unknown causes. Studies on differences between epidemic and circulating endemic strains of Shigella are scarce.…”

Section: Introductionmentioning

confidence: 99%

Differential Host Immune Responses to Epidemic and Endemic Strains of Shigella dysenteriae Type 1

Sayem

Ahmad

Rekha

et al. 2011

J Health Popul Nutr

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Shigella dysenteriae type 1 causes devastating epidemics in developing countries with high case-fatality rates in all age-groups. The aim of the study was to compare host immune responses to epidemic (T2218) and endemic strains of S. dysenteriae type 1. Shigellacidal activity of serum from rabbits immunized with epidemic or endemic strains, S. dysenteriae type 1-infected patients, and healthy adult controls from Shigella endemic and non-endemic regions was measured. Immunogenic cross-reactivity of antibodies against Shigella antigens was evaluated by Western blot analysis. Oxidative burst and phagocytic responses of monocytes and neutrophils to selected S. dysenteriae type 1 strains were assessed by flow cytometry. Rabbit antisera against epidemic strain were less effective in killing heterologous bacteria compared to endemic antisera (p=0.0002). Patients showed an increased serum shigellacidal response after two weeks of onset of diarrhoea compared to the acute stage (3-4 days after onset) against their respective homologous strains; the response against T2218 and heterologous endemic S. dysenteriae type 1 strains was not significant. The serum shigellacidal response against all the S. dysenteriae type 1 strains was similar among healthy controls from endemic and non-endemic regions and was comparable with the acute stage response by patients. Compared to endemic strains of S. dysenteriae type 1, T2218 was significantly resistant to phagocytosis by both monocytes and neutrophils. No obvious differences were obtained in the induction of oxidative burst activity and cathelicidin-mediated killing. Cross-reactivity of antibody against antigens present in the epidemic and endemic strains showed some differences in protein/peptide complexity and intensity by Western blot analysis. In summary, epidemic T2218 strain was more resistant to antibody-mediated defenses, namely phagocytosis and shigellacidal activity, compared to endemic S. dysenteriae type 1 strains. Part of this variation may be attributed to the differential complexity of protein/peptide antigens.

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Section: Introductionmentioning

confidence: 99%

Differential Host Immune Responses to Epidemic and Endemic Strains of Shigella dysenteriae Type 1

Sayem

Ahmad

Rekha

et al. 2011

J Health Popul Nutr

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“…Specific and type-specific immunity to Shigella infection is acquired after dysentery but is relatively weak and for a short duration. Therefore, the disease may recur many times due to drug resistance and in some cases, may become chronic (Hens et al, 2005). Targeting host cellular receptors in order to induce typespecific humoral or cellular immune response could be beneficial in achieving immunity to shigellosis and overcome the disease burden in developing countries.…”

Section: Introductionmentioning

confidence: 99%

Host Receptor Immunomodulation in Response to Shigella Surface Antigens: An Insight for Vaccine Development

Bagchi¹,

Bagchi²,

Hens³

et al. 2015

American Journal of Immunology

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Shigellosis, caused by Shigella is the most common cause of bacillary dysentery. The disease is associated with high morbidity and mortality rate owing to its multiple drug resistance. Hence recovery from the disease would primarily depend on the development of an effective immune-modulator for strong mucosal immune response. The role of cellular immunity may be a critical factor in protection against shigellosis as Shigella remains an intracellular pathogen during most of its life-cycle. Development of a potent immunomodulator may provide strong and longlasting immunity to shigellosis. In this review, we have attempted to highlight the disease dimension and its deviation due to the effect of various Shigella surface antigens that would help in the development of an effective immune response. Cellular innate immune modulation will be a new generation target for the development of mucosal candidate vaccines where proper receptor activation such as Toll-Like Receptors (TLRs), Cytokine Receptors (CyRs) and/or T-Cell Receptors (TCRs) on the host cell could be aimed at producing mucosal immunity. An effort has been made to better understand the effect of these immunomodulators against shigellosis by way of modulating the host immune mechanism to Shigella outer membrane component.

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New temperate DNA phage BcP15 acts as a drug resistance vector

Hens¹,

Chatterjee

Kumar

2006

Arch Virol

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This study was designed to determine the role of a new temperate DNA phage BcP15 in relation to drug resistance. The multidrug resistant Shigella flexneri NK1925 was isolated from a patient of Infectious Diseases Hospital, Kolkata, India. This strain contained five plasmids ranging in size from 3 to 212 kb. After curing of five plasmids, this strain became sensitive to antibiotics. A plasmidless multidrug-resistant strain Burkholderia cepacia DR11 was isolated during the survey of microorganisms from coastal waters of deltaic Sunderbans. This strain always released a temperate phage BcP15 into culture supernatant. Turbid plaque formation was observed on the lawn of a plasmidless version (Pl(-)35) of Shigella flexneri NK1925. A few distinct clones (Pl(-)35R) appeared within the region of each plaque after 18 h incubation. S. flexneri NK1925, Pl(-)35, and Pl(-)35R clones showed the same PFGE band pattern of XbaI-digested chromosomal DNA. However, Pl(-)35R clones were resistant to co-trimoxazole, trimethoprim, and eryth- romycin, to which B. cepacia DR11 was also resistant. Southern hybridization results indicated that these three antibiotic resistances in Pl(-)35R clones were due to a BcP15 phage lysogen in the Pl(-)35 version of S. flexneri NK1925.

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Epidemic Strain Shigella dysenteriae Type 1 Dt66 Encodes Several Drug Resistances by Chromosome

Cited by 5 publications

References 28 publications

Differential Host Immune Responses to Epidemic and Endemic Strains of <i>Shigella dysenteriae <i> Type 1

Differential Host Immune Responses to Epidemic and Endemic Strains of <i>Shigella dysenteriae <i> Type 1

Host Receptor Immunomodulation in Response to <i>Shigella</i> Surface Antigens: An Insight for Vaccine Development

New temperate DNA phage BcP15 acts as a drug resistance vector

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